http://www.cnr.it/ontology/cnr/individuo/prodotto/ID20908
17-beta estradiol induces spermatogonial proliferation through Mitogen Activated Protein Kinase (Extracellular Signal Regulated Kinase 1/2) activity in the lizard (podarcis s. Sicula) (Articolo in rivista)
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- 17-beta estradiol induces spermatogonial proliferation through Mitogen Activated Protein Kinase (Extracellular Signal Regulated Kinase 1/2) activity in the lizard (podarcis s. Sicula) (Articolo in rivista) (literal)
- Anno
- 2002-01-01T00:00:00+01:00 (literal)
- Alternative label
Chieffi P. 1-2, Colucci- D'Amato G.L. 2-3, Guarino F. 4, Salvatore G. 5, Angelini F. 4 (2002)
17-beta estradiol induces spermatogonial proliferation through Mitogen Activated Protein Kinase (Extracellular Signal Regulated Kinase 1/2) activity in the lizard (podarcis s. Sicula)
in Molecular reproduction and development
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Chieffi P. 1-2, Colucci- D'Amato G.L. 2-3, Guarino F. 4, Salvatore G. 5, Angelini F. 4 (literal)
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- Titolo
- 17-beta estradiol induces spermatogonial proliferation through Mitogen Activated Protein Kinase (Extracellular Signal Regulated Kinase 1/2) activity in the lizard (podarcis s. Sicula) (literal)
- Abstract
- There are always more evidences indicating that 17beta-estradiol (E(2)) is necessary for normal male fertility. We have used a nonmammalian vertebrate model (the lizard Podarcis s. sicula) to investigate the regulation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) activity in the testis during the annual sexual cycle and to study whether E(2) exerts a role in the spermatogenesis through ERK1/2 activity. Immunocytochemistry analysis shows that ERK1/2 proteins are present in the nucleus of the spermatogonia (SPG), and in primary (I) spermatocytes (SPC). The annual E(2) profile shows a progressive increase during the active spermatogenesis (from April to June) and a peak in the month of August (spermatogonial mitosis). In parallel, ERK1/2 (molecular weight 44 and 42 kDa, respectively) are highly phosphorylated during the period of active spermatogenesis and in post-refractory period (August) compared with the winter stasis (from November to March). Present results demonstrate that E(2) treatment induces spermatogonial proliferation, possibly via the activation of ERK1/2, and this effect is counteracted by the antiestrogen ICI 182-780. (literal)
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